Size-related and size-unrelated functional heterogeneity among pancreatic islets

Aizawa, Toru; Kaneko, Tsuyoshi; Yamauchi, Kazuyo; Yajima, Hiroki; Nishizawa, Tomoko; Yada, Toshihiko; Matsukawa, Hiroshi; Nagai, Minoru; Yamada, Satoko; Sato, Yoshihiko; Komatsu, Mitsuhisa; Itoh, Nobuo; Hidaka, Hiroya; Kajimoto, Yoshitaka; Hashizume, Kiyoshi

doi:10.1016/s0024-3205(01)01332-7

Cited by 22 publications

(24 citation statements)

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“…Some islets show a typical biphasic response, but many others show either predominant first-or secondphase responses (6). This finding agrees well with the electrophysiological heterogeneity of individual rat islets (7).…”

Section: Recognition Of Biphasic Insulin Release Upon a Square-wave Asupporting

confidence: 88%

“…Recent studies on membrane potential and [Ca 2ϩ ] i changes in rat ␤-cells clearly revealed that the temporal profiles of ionic events during the second phase do not coincide with a gradually increasing pattern of insulin secretion (7). Namely, the depolarization, number of action potentials, ] i during the second phase all remained stable (6). Therefore, a biphasic insulin release upon glucose stimulation cannot be simply explained by the K ATP channel closure and subsequent elevation of [Ca 2ϩ ] i .…”

Section: Underlying Signals For Biphasic Insulin Secretionmentioning

confidence: 97%

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Importance of Nonionic Signals for Glucose-Induced Biphasic Insulin Secretion

Aizawa

Sato²,

Komatsu³

2002

Diabetes

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Glucose induces biphasic insulin secretion by the islet ␤-cell. Based on recent knowledge on glucose signaling in the ␤-cell, the underlying mechanisms for this biphasicity could be envisaged as follows. Glucose-induced elevation of cytosolic free Ca 2؉ concentration, which is due to the electrophysiological events that originate in closure of the ATP-sensitive K ؉ (K ATP ) channel, most likely triggers the first phase. The second phase is produced by gradual augmentation and potentiation of Ca 2؉ -triggered insulin release by the K ATP channelindependent, nonionic signals. Protein acylation may be involved in the nonionic signaling. In patients lacking functional K ATP channels, however, the first phase of glucose-induced insulin secretion is clearly retained, casting doubt on the simplistic view outlined above. In this pathological condition, the K ATP channel-independent, most likely nonionic, glucose action alone is sufficient for the first-phase response. Diabetes 51 (Suppl.

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Section: Recognition Of Biphasic Insulin Release Upon a Square-wave Asupporting

confidence: 88%

Section: Underlying Signals For Biphasic Insulin Secretionmentioning

confidence: 97%

Importance of Nonionic Signals for Glucose-Induced Biphasic Insulin Secretion

Aizawa

Sato²,

Komatsu³

2002

Diabetes

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“…There is size-related and size-unrelated functional diversity among pancreatic islets [26,27]. Only 60% islets responded to high glucose in a concentration-dependent and 32% in an all-or-none manner, and 8% islets did not respond at all [26].…”

Section: Discussionmentioning

confidence: 99%

Cell Swelling-induced Insulin Secretion from INS-1E Cells is Inhibited by Extracellular Ca<sup>2+</sup> and is Tetanus Toxin Resistant

Orečná

Hafko

Toporcerová

et al. 2010

Cell Physiol Biochem

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Cell swelling-induced insulin secretion represents an alternative pathway of stimulation of insulin secretion. INS-1E rat tumor beta cells do not release insulin in response to cell swelling in presence of Ca²⁺ despite a good response to glucose challenge and appropriate increase in cell volume. Surprisingly, perifusion with Ca²⁺-depleted medium showed distinct secretory response of INS-1E cells to hypotonicity. Objective of this study was further characterization of the role of Ca²⁺ in secretory process in INS-1 and INS-1E cell lines. Ca²⁺ depleted hypotonic medium with 10 µM BAPTA/AM (intracellular chelator) induced insulin secretion from both types of cells. We demonstrated expression of L-type Ca²⁺ channel Ca_v1.2 and non-L-type Ca²⁺ channels Ca_v2.1 (P/Q-type), Ca_v2.2 (N-type), and Ca_v3.1 (T-type) in both cell lines. Inhibition of L type channel with nifedipine and/or P/Q type with ω-agatoxin IVA enabled distinct response to hypotonic medium also in INS-1E cells. Tetanus toxin (TeTx) in medium containing Ca²⁺ and a group of calcium channel blockers inhibited hypotonicity-induced insulin secretion from INS-1 cells but not from INS-1E cells. Conclusion: Hypotonicity-induced insulin secretion from INS-1E cells is inhibited by extracellular Ca²⁺, does not require intracellular Ca²⁺ and is TeTx resistant.

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“…28,29 Heterogeneity between islets has also been demonstrated with some characteristics associated with islet size. 30 For example, previous studies concluded that small islets relied solely on voltagegated calcium channels for insulin release, while large islets were less dependent. 30 The shortage of donors and the exceptional amount of tissue necessary for successful islet transplants limits the procedure's usefulness as a widely-available therapeutic intervention.…”

mentioning

confidence: 99%

“…30 For example, previous studies concluded that small islets relied solely on voltagegated calcium channels for insulin release, while large islets were less dependent. 30 The shortage of donors and the exceptional amount of tissue necessary for successful islet transplants limits the procedure's usefulness as a widely-available therapeutic intervention. While stem cells or animal sources may eventually produce unlimited supplies of tissue for transplant, improved understanding of islet biology will allow more rapid adjustments in the current transplant procedure that may improve outcomes since a loss of islets after isolation is commonly observed, 31 and negatively affects transplant outcomes.…”

mentioning

confidence: 99%